Darwinism as an explanation for life is dead. The final death blow was administered by discoveries about intracellular nanomachinery, which amply satisfy Darwin's own test of falsification.
Dead, but it won't lie down. Evolutionism is propped up by the well organised and well funded enemies of Biblical Christianity as it is foundational to the secular humanist world view they hold so dear. This blog will criticise evolutionism and explore its harmful effects.

Tuesday, 26 August 2014

Michael Behe refuted-no, not at all

Whenever I quote Michael Behe to atheists/evolutionists on irreducible complexity or intelligent design, I get a derisive snort and one of two responses (often both)

'Behe has been refuted- many, many times.'

or 'Behe got his ass whipped at Dover.'

Neither of these standard assertions are remotely true, they are just knee jerk responses, memes if you like, inculcated by the restless and determined 'There is no evidence against evolution' activists. Anyhow, recent publications (see link) have further justified Behe's thesis that natural selection acting on random mutations simply does not have the creative or explanatory powers required for unguided molecules to man evolution to have occured. A short essay setting this out is reproduced below, courtesy of Professor Behe and the Centre for Intelligent Design.

Behe is right. He has quite simply falsified evolution's fundamental mechanism at the most profound biochemical level. No wonder those whose world view depends on evolution being true hate him.

Evolution's Lottery

"Evolution
is like the National Lottery - a lot of people buy tickets, and almost
everyone loses.

Imagine
a weekly lottery game where a card has eight windows, each with a flap
covering a single digit from zero to nine. If, when revealed, all the digits
match each other (ten ways to win!) the player receives £1,000,000. It would
be very unlikely that anyone in a village of a thousand would win even if all
the people played, because the chances of eight random digits matching each
other are one in ten million. In fact, all the people in the village would
have to play the game over and over again for centuries before anyone there
would be expected to win. Yet if everyone in the whole of Britain played,
we'd expect about a half-dozen winners each week, because there would be many
more chances for someone to have a winning ticket.

Now
think of a super lottery, where the prize is £1,000,000,000,000 - more than
the national budget. In order to win this game, a player has to buy two
eight-window tickets, and, as before, the numbers on both tickets have to
match each other. How long would it take for a player in Britain to win? If
you do the arithmetic, it would take about 30,000 years for anyone at all to
win. Most people would likely give up and play a different game.

The
game of evolution depends on the same two factors as the National Lottery:
the odds of winning and the number of players. But instead of matching
numbers on a card, evolution has to match the right mutations to an
organism's DNA. As an example, consider one of the gravest threats to human
health - malaria. The malaria parasite is a tiny single-cell organism that is
transmitted by the bite of an infected mosquito. Once it enters a human, a
malaria cell multiplies by eating her blood, which often kills the victim.
For thousands of years humans have had little defense against the disease. In
the past century, however, antibiotic drugs have been developed that kill
malaria.

To
understand the malaria evolution lottery, let's look at two drugs. The first
is called atovaquone. Atovaquone readily kills normal malaria cells - in a
laboratory, adding the drug to a flask that contains millions of such cells
will usually wipe them out. Yet if the drug is given to a person suffering
from malaria, it often fails. Why? It turns out that, although malaria needs
just one particular mutation in its DNA to gain resistance to atovaquone, the
likelihood of the mutation occurring is about one in a hundred million cells.
Since there are only a few million cells in the lab flask, the odds are poor
that any of them will have the right mutation, so the drug kills them all. A
person sick with malaria, however, can harbor up to a million million cells.
Like the example above of the UK vs a single village, the greater numbers
make the odds very good that one or more of those cells will have the winning
ticket. So malaria seems to develop resistance easily in patients treated
with atovaquone, even though the mutation itself is quite unlikely.

The
second drug is called chloroquine. Instead of resistance appearing in every
few patients as with atovaquone, new malarial resistance to chloroquine only
appears once in about every hundred million patients. What could account for
this astounding difference in frequency? In my 2007 book The Edge of
Evolution I argued that the logic of the lottery example could easily explain
it. If instead of one particular mutation, malarial resistance to chloroquine
needed two particular mutations to occur in the same cell, the likelihood of
getting them both would be drastically less than getting an individual
mutation. Instead of one in a hundred million, resistance would appear in
only one of every ten thousand million million. Since that astronomical
number is much greater than the number of malaria cells in a single patient,
almost all patients would be cured by chloroquine. (Regrettably, in the very
large number of patients on earth who become sick, there are enough malaria
cells to yield a few that do have resistance to chloroquine. The growth of
those few and their dissemination by mosquitoes have caused chloroquine
resistance to become common.)

Recent
scientific results have confirmed that at least two mutations are indeed
needed for chloroquine resistance, as I predicted. This teaches us several
important lessons about evolution, one practical and one theoretical. The
practical lesson is that disease microbes like malaria can be stopped if we
find a drug or combination of drugs that would require multiple mutations to
overcome them. Evolution isn't the relentless force that Darwinists have
often portrayed - there exists an edge beyond which it becomes helpless, as
intelligent design proponents expected.

The
theoretical lesson is that, just as with battling microbes, we should expect
there to be an edge to random evolution in the history of life, too. Yes,
chance mutations plus natural selection do explain some features of biology.
But if even several mutations were needed together to produce some complex
organ or feature of life, it becomes much less likely that unguided natural
processes explain it.

Do
many features of life require multiple mutations? Almost all functional ones
do. The basic machines of life are constructed of molecules called proteins,
and proteins themselves are typically made of hundreds of units of amino
acids joined together. Those machines, under the guidance of complex
instructions encoded in an organism's DNA, build the plants and animals we
know. At some point in the history of life each of those amino acids in each
of the protein machines had to have been new - a mutation. So virtually all
proteins, as well as the complex instruction sets controlling them, are
beyond the edge of random evolution.

What's
more, although tiny organisms such as malaria have the huge population
numbers to allow them to overcome small evolutionary roadblocks such as
presented by chloroquine, larger organisms don't. Larger organisms are
unlikely to win an evolutionary lottery at all if it needs just two or more
mutations. The conclusion is that very little of what we see in life can be
the result of the random processes invoked by Darwinian evolution. Rather,
almost all features of life required purposeful intelligent design."

If you have any questions on the
above, you can contact Mike Behe directly atmjb1@Lehigh.EDU.